The Effect of Cigarette Smoke Exposure on Efferocytosis in Chronic Obstructive Pulmonary Disease; Molecular Mechanisms and Treatment Opportunities

Chitosan-Coated Solid Lipid Nano-Encapsulation Improves the Therapeutic Antiairway Inflammation Effect of Berberine against COPD in Cigarette Smoke-Exposed Rats

“…Inflammation and oxidative stress are known to play a key role in COPD pathogenesis [50]. Neutrophils and macrophages are the main innate immune cells that infiltrate the lungs and participate in the pathogenesis of CS-induced COPD through inflammation and direct induction of endothelial and epithelial cell death [20,51,52]. Neutrophils have been detected to be increased in the small airways of COPD patients [53].…”

“…Neutrophils have been detected to be increased in the small airways of COPD patients [53]. Inflammatory alveolar macrophages tend to express inflammatory cytokines and secrete matrix metalloproteases, and activated neutrophils are recruited to the airways and release reactive oxygen species (ROS) and neutrophil elastase, causing an injury to the epithelium and underlying basement membrane in the lung tissues and leading to COPD progression [20,51,52,54]. Such inflammatory cells can also promote immune responses, leading to an elevation in levels of inflammatory cytokines, which intensify the inflammatory response and exert a key role in the airway inflammation in COPD by recruiting inflammatory cells and airway hyper-responsiveness [55][56][57][58][59][60][61][62][63][64][65].…”

The regulation of efferocytosis signaling pathways and adipose tissue homeostasis in physiological conditions and obesity: Current understanding and treatment options

“…These events prevent the destruction of cells and the release of inflammatory contents. At the conclusion of efferocytosis, efferocytes release macrophage tumor growth factor beta (TGF‐ β ) and IL‐10 as anti‐inflammatory responses that result in control of inflammation 18,22,25,29–31 (Table 1 and Figures 1 and 2). In obesity, the engulfment step is very important in AT and macrophages regulate tissue homeostasis by the uptake and degradation of lipoproteins in plasma 32 .…”

“…Clearance of the ACs by efferocytosis without inflammation is effective in preventing necrosis and the release of pro‐inflammatory tissue‐damaging cell contents, such as damage‐associated molecular pattern (DAMP) molecules 18–20 . The phagocytosis of ACs causes the expression of phagocytic receptors; this, in turn, leads to an additional metabolic load in the phagocytic cell and, as a consequence, the improper clearance of ACs leads to chronic inflammatory diseases, such as obesity, inflammatory lung diseases, autoimmune and neurological disorders, T2D, and atherosclerosis 18,21–25 …”

“…[18][19][20] The phagocytosis of ACs causes the expression of phagocytic receptors; this, in turn, leads to an additional metabolic load in the phagocytic cell and, as a consequence, the improper clearance of ACs leads to chronic inflammatory diseases, such as obesity, inflammatory lung diseases, autoimmune and neurological disorders, T2D, and atherosclerosis. 18,[21][22][23][24][25] According to published studies, obesity can impact efferocytosis. [26][27][28] Obesity, together with defective efferocytosis, is also associated with other diseases, such as asthma and cancer.…”